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Nasal administration of transforming growth factor-ß1 induces dendritic cells and inhibits protracted-relapsing experimental allergic encephalomyelitis

Division of Neurology, Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden

Yuxuen Jin

Division of Neurology, Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden, Department of Neurology, Huashan Hospital, Shanghai Medical University, Shanghai, P.R. China

Hong Guo

Division of Neurology, Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden, Department of Neurology, Beijing Hospital, Ministry of Health, Beijing, P.R. China

Hans Link

Division of Neurology, Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden

Bao-Guo Xiao

Division of Neurology, Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden

Cytokines have a crucial role in initiation and perturbation of EAE that represents an animal model of multiple sclerosis (MS). Administration of transforming growth factor-ß1 (TGF-ß1) to EAE mice improves clinical EAE and prevents relapses by unknown mechanisms. Administering low doses of TGF-ß1 nasally, we confirmed that TGF-ß1 inhibited development and relapse of protracted-relapsing EAE (PR-EAE) in DA rats. Infiltration of CD4+ T-cells and macrophages within the central nervous system was clearly reduced, while proliferation and IFN-g secretion of mononuclear cells (MNC) was augmented in TGF-ß1-treated EAE rats compared to PBS-treated control EAE rats. TGF-ß1 administered nasally also increased nitric oxide production and CD4+ T cell apoptosis. TGF-ß1 treated rats showed augmented proliferation of dendritic cells (DC) compared to MNC. These data imply that low doses of TGF-ß1 given by the nasal route prevent PR-EAE and upregulate DC functions that may be involved for disease prevention.

Key Words: transforming growth factor-ß • dendritic cell • intranasal immunotherapy • experimental allergic encephalomyelitis • multiple sclerosis • apoptosis

Multiple Sclerosis, Vol. 5, No. 3, 184-191 (1999)
DOI: 10.1177/135245859900500308


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